Background:. Expression of matrix metalloproteinase (MMP) has been shown in aortic dissection and aneurysms indicating increased proteolysis compared w

An athlete's heart is characterized by morphological and functional changes occurring as a consequence of regular physical exercise. We sought to determine if these physiological changes lead to ventricular repolarization abnormalities in trained athletes. Forty-four trained athletes and 35 sex- and age-matched healthy sedentary controls were included in the study. A 12-lead surface electrocardiogram (ECG) was obtained from all participants. Maximum QT (QTmax) and minimum QT (QTmin) interval durations, QT dispersion (QTd) and corrected QT dispersion (QTcd) were calculated for each ECG record. Heart rate, systolic and diastolic blood pressure values were found to be identical in both groups. QTmax and QTmin interval durations were not statistically different between the athletic and control groups. Similarly, QTd and QTcd did not differ significantly between the two groups. No association was observed between an athlete's heart and ventricular heterogeneity compared with healthy sedentary controls, despite physiological and structural changes.

Liver transplantation (LT) is a key treatment for primary and secondary liver cancers, reducing tumor burden with concurrent improvement of liver function. While significant improvement in survival is noted with LT, cancer recurrence rates remain high. Mitochondrial dysfunction caused by ischemia-reperfusion injury (IRI) is known to drive tumor recurrence by creating a favorable microenvironment rich in pro-inflammatory and angiogenic factors. Therefore, strategies that decrease reperfusion injury and mitochondrial dysfunction may also decrease cancer recurrence following LT. Machine perfusion techniques are increasingly used in routine clinical practice of LT with improved post-transplant outcomes and increased use of marginal grafts. Normothermic (NMP) and hypothermic oxygenated machine perfusion (HOPE) provide oxygen to ischemic tissues, and impact IRI and potential cancer recurrence through different mechanisms. This article discussed the link between IRI-associated inflammation and tumor recurrence after LT. The current literature was screened for the role of machine perfusion as a strategy to mitigate the risk of cancer recurrence. Upfront NMP (“ischemia free organ transplantation”) and end-ischemic HOPE were shown to reduce hepatocellular carcinoma recurrence in retrospective studies. Three prospective randomized controlled trials are ongoing in Europe to provide robust evidence on the impact of HOPE on cancer recurrence in LT.

Machine perfusion technologies have redefined the landscape of organ preservation by enabling not just static cold storage, but graft optimization and assessment with the opportunity for additional therapeutic interventions. Preservation solutions, traditionally developed for static cold storage, are now being adapted for use in dynamic perfusion platforms. The optimal composition for machine perfusion remains unclear as we shift to creating biologically intelligent platforms tailored to mitigate ischemia–reperfusion injury. This review presents a mechanistic framework for understanding organ preservation through the lens of shared vulnerabilities, particularly: mitochondrial dysfunction, endothelial barrier breakdown, and the activation of inflammatory cascades. We discuss the evolution of classical preservation solutions, the rationale for redox-targeted and endothelial-stabilizing additives, and the promise of modular approaches adaptable to both static cold storage and machine perfusion. By integrating recent preclinical insights, systems biology, and emerging clinical trials, we outline the path toward unified, precision-preservation strategies capable of expanding the donor pool and improving transplant outcomes.

Liver transplantation is known to generate significant inflammation in the entire organ based on the metabolic profile and the tissue’s ability to recover from the ischemia-reperfusion injury (IRI). This cascade contributes to post-transplant complications, affecting both the synthetic liver function (immediate) and the scar development in the biliary tree. The new occurrence of biliary strictures, and the recurrence of malignant and benign liver diseases, such as cholangiocarcinoma (CCA) and primary sclerosing cholangitis (PSC), are direct consequences linked to this inflammation. The accumulation of toxic metabolites, such as succinate, causes undirected electron flows, triggering the releases of reactive oxygen species (ROS) from a severely dysfunctional mitochondrial complex 1. This initiates the inflammatory IRI cascade, with subsequent ischemic biliary stricturing, and the upregulation of pro-tumorigenic signaling. Such inflammation is both local and systemic, promoting an immunocompromised status that can lead to the recurrence of underlying liver disease, both malignant and benign in nature. The traditional treatment for CCA was resection, when possible, followed by cytotoxic chemotherapy. Liver transplant oncology is increasingly recognized as a potentially curative approach for patients with intrahepatic (iCCA) and perihilar (pCCA) cholangiocarcinoma. The link between IRI and disease recurrence is increasingly recognized in transplant oncology for hepatocellular carcinoma. However, smaller numbers have prevented similar analyses for CCA. The mechanistic link may be even more critical in this disease, as IRI causes the most profound damage to the intrahepatic bile ducts. This article reviews the underlying mechanisms associated with biliary inflammation and biliary pathology after liver transplantation. One main focus is on the link between transplant-related IRI-associated inflammation and the recurrence of cholangiocarcinoma and benign liver diseases of the biliary tree. Risk factors and protective strategies are highlighted.

Ex situ machine perfusion has emerged as a pivotal technique for organ preservation and pre-transplant viability assessment, where the real-time monitoring of mitochondrial biomarkers—flavin mononucleotide (FMN) and nicotinamide adenine dinucleotide (NADH)—could significantly mitigate ischemia-reperfusion injury risks. This study develops a non-invasive optical method combining fluorescence and UV-visible spectrophotometry to quantify FMN and NADH in hypothermic oxygenated perfusion media. Calibration curves revealed linear responses for both biomarkers in absorption and fluorescence (FMN: λ_ex = 445 nm, λ_em = 530–540 nm; NADH: λ_ex = 340 nm, λ_em = 465 nm) at concentrations < 100 μg mL⁻¹. However, NADH exhibited nonlinear fluorescence above 100 μg mL⁻¹, requiring shifted excitation to 365 nm for reliable detection. Spectroscopic analysis further demonstrated how perfusion solution composition alters FMN/NADH fluorescence properties, with consistent reproducibility across media. The method’s robustness was validated through comparative studies in clinically relevant solutions, proposing a strategy for precise biomarker quantification without invasive sampling. These findings establish a foundation for real-time, optical biosensor development to enhance organ perfusion monitoring. By bridging spectroscopic principles with clinical needs, this work advances translational sensor technologies for transplant medicine, offering a template for future device integration.